The major role of sympathoadrenal mechanisms in maintaining cardiovascular homeostasis during hypoxemia in postnatal life is well known. Sufficient work has been done to confirm the importance of the sympathoadrenal system in the fetal response to hypoxemic stress as well, but the function of this system in the fetus is poorly understood in many details. For this reason further study is planned in this field with a concentration in the current project in the area of fetal adrenal medullary function. Experiments will be performed in chronically prepared pregnant sheep and will be based to a large extent on the chronic fetal adrenal cannula method developed in our laboratory. This method allows the direct determination of fetal adrenal secretion of catecholamines which will be correlated with levels of fetal oxygenation and with fetal hemodynamic parameters. More specifically, basic mechanisms, neural and direct, involved in control of adrenal secretion of catecholamines by the fetus will be explored. Further, the roles of such factors as pH, PO2 and Cao2 in activating those mechanisms and the possible role of endogenous opiates as modifiers of fetal medullary secretion will be investigated. In other experiments, the effects of repeated bouts of hypoxemia and of prolonged, sustained oxygen deprivation on fetal adrenal medullary function will be determined. Either exhaustion or enhancement of glandular function could be the consequence of such stress. The importance of the adrenal medulla in maintaining both normal circulating levels of catecholamines and hemodynamic stability will be defined by studies in fetuses following ablation of the adrenal medulla. Finally, the interplay between fetal adrenergic innervation and adrenal medullary function will be examined by observing adrenal secretion of catecholamines at rest and in response to hypoxemic stress in fetuses with chemical sympathectomy.